INTRAVITREAL INJECTION OF GANGLIOSIDE GM1 AFTER ISCHEMIA REDUCES RETINAL DAMAGE IN RATS

Background and Purpose Gangliosides are normal components of cell memb ranes and contribute to structural rigidity and membrane function. The y have been shown to protect against various insults in the brain. We have shown previously that GM1 administered intraperitoneally before t he induction of retinal ischemia provides a protective effect. This st udy evaluates the protective effect of GM1 administered intravitreally after ischemia on retinal lesions. Methods We induced retinal ischemi a unilaterally in Long-Evans rats by increasing intraocular pressure t o 160 mm Hg for 60 minutes. GM1 (20 mu L . 10(-5) mol/L) or saline (20 mu L) was injected into the vitreous 15 minutes after ischemia, and t he postischemic survival time was either 8 or 15 days. The degree of r etinal damage was assessed by histopathological study. Results Retinal ischemia led to reductions in thickness and cell number, principally in the inner retinal layers (39% to 80%) and to a lesser extent in the outer retinal layers (26% to 45%). Postischemic treatment with intrav itreally injected GM1 conferred significant protection against retinal ischemic damage after both 8 and 15 days of survival time. After 8 da ys of reperfusion, the ischemia-induced loss in overall retinal thickn ess was reduced by 15% and those of the inner nuclear and plexiform la yers by 44% and 17%, respectively. Ischemic-induced ganglion cell and inner nuclear cell density losses were reduced by 37% and 27%, respect ively. After 15 days of reperfusion, approximately the same statistica lly significant differences could be observed in comparison with the 1 5-day saline-injected group. Conclusions GM1 protects the rat retina f rom pressure-induced ischemic injury when given intravitreally after t he insult. The protection provided by GM1 after initiation of retinal damage could be of therapeutic interest.